Andrew F. Bent

Andrew F. Bent was born in Springfield, Ohio. He obtained a B.A. in Biology, magnum cum laude, from Oberlin College in 1983 and a Ph.D. from MIT in 1989. Following post-doctoral work at the University of California-Berkeley he joined the faculty at the University of Illinois in 1994. In 1999 he moved to the University of Wisconsin-Madison, where he is Professor of Plant Pathology. His previous awards include the UW-Madison Pound Award for Excellence in Research, the APS Noel T. Keen Award for Research Excellence in Molecular Plant Pathology, and Fellow of the American Association for the Advancement of Science. Professor Bent is widely recognized for his internationally renowned research, which has significantly advanced our knowledge of the molecular mechanisms underlying plant disease resistance. Specifically, Bent has made multiple important discoveries about pathogen recognition, the signaling events leading to defense activation, and the host defenses that are induced. His research has focused both on the model plant Arabidopsis and on soybean, one of the world’s most important food crops.

While a postdoctoral scientist Bent was co-first author of a widely cited paper that launched the Arabidopsis-Pseudomonas interaction as an experimental system (Plant Cell 3:49-59, 1991). Significant discoveries in plant pathology continue to emerge from this pathosystem. Bent was then lead author on the first report that plant disease resistance genes (R genes) often encode NB-LRR proteins, a discovery that launched a new era of understanding how plant resistance genes function (Science 265:1856-1860, 1994).

In 1998, Bent and colleagues significantly refined Agrobacterium-based methods to genetically transform Arabidopsis without tissue culture. This "floral dip" Arabidopsis transformation protocol proved so successful that the corresponding paper (Plant Journal 16:735-743) is one of the most highly cited in plant biology, with over 12,000 citations. More importantly, the method enabled advances in many areas of plant biology and facilitated creation of exhaustive sequence-indexed T-DNA insertion mutant collections. The Bent lab also discovered mechanisms that underpin this floral dip transformation method (Plant Physiology 123:895-904, 2000).

Between 1998 and 2008, Bent and his group dissected plant disease resistance and the hypersensitive resistance response using a class of Arabidopsis mutants known as “defense, no death” (dnd) (PNAS 95:7819-7824, 1998; PNAS 97:9323-9328, 2000; MPMI 21:1285-1296, 2008). This approach elegantly separated the phenomenon of R gene-mediated (gene-for-gene) resistance from cell death per se. This work also showed that the independently identified dnd1 and dnd2 genes both encode mutated cyclic nucleotide-gated ion channels that contribute to plant defense activation.

Bent’s work with Arabidopsis and soybean also demonstrated roles for ethylene in disease tolerance and disease resistance (MPMI 5:372-378, 1992; Plant Physiology 119:935-950, 1999). In 2006 his group published a paper on soybean research that was noteworthy as a rare instance in which molecular host defense dissection was extended to field studies (Crop Science 46:893-901).

In the past decade the Bent group has made substantial contributions in three areas. First are discoveries regarding the structure and function of the plant pattern recognition receptors that activate defense responses after detecting microbe-associated molecular patterns (MAMPs, also known as PAMPs). They demonstrated that MAMPs are not always highly conserved; even within a single bacterial pathogen species, different strains can carry flagellins that are or are not recognized by the FLS2 flagellin receptor (Plant Cell 18:764-779, 2006). That work also identified the recognition-determining flagellin polymorphism. The Bent lab then identified the binding site for flagellin in the LRR (leucine-rich repeat) domain of FLS2 (Plant Cell 19:3297-3313, 2007). They also identified multiple other functional details regarding FLS2 phosphorylation, glycosylation, and protein-protein interactions (Plant Cell 24:1096-1113, 2012;
PLoS Pathogens 9:e1003313, 2013; PLoS ONE 9:e111185, 2014), released a web-based server for discovery of conserved surface regions (predicted functional sites) of LRR domains (PLoS ONE 6:e21614, 2011), and demonstrated early approaches to in vitro evolution of plant immune receptors to new pathogen recognition specificities (PLoS ONE 11:e0157155, 2016).

Bent’s second main area of recent research has revealed that poly-ADP-ribosylation, a posttranslational protein modification well known in mammalian responses to DNA damage, plays significant roles in plant responses to infection. As part of this work, Bent and colleagues made the foundational discovery that microbial infections can cause double-strand breaks in host plant DNA early in the infection process (PLoS Pathogens 10:e1004030, 2014). They also demonstrated that plants rely primarily on a different PARP enzyme than mammals (one with different domain structures), and that this PARP2 mediates beneficial plant responses to pathogens and to abiotically induced DNA damage (PLoS Genetics 11:e1005200, 2015).

In a third major research focus, Bent has led discoveries about the soybean Rhg1 locus, which is widely used in soybean cultivars for resistance to soybean cyst nematode, the most economically significant pathogen of soybean worldwide. His group molecularly isolated Rhg1 and discovered gene copy number variation as a mechanism for the emergence of disease resistance (Science 338:1206-1209, 2012). The most widely used version of Rhg1 carries ten direct repeat copies of a four-gene block, with three disparate proteins encoded at Rhg1 each contributing to cyst nematode resistance. Excitingly, in 2016 Bent’s group uncovered a new mechanistic paradigm of plant disease resistance: a dysfunctional version of a core cellular housekeeping protein (PNAS 113:E7375-E7382, 2016). They found that in syncytia (plant cells that nematodes have reprogrammed to support nematode growth), an Rhg1-encoded dysfunctional version of the core plant housekeeping protein alpha-SNAP degrades the biotrophic interface between plant and nematode by disrupting vesicular trafficking machinery. This exciting discovery is only the latest in a consistently productive career arc that continues upward.

Bent is an enthusiastic and effective teacher of advanced courses in plant disease resistance breeding and in molecular plant-microbe interactions, as well as biology for non-science majors. His textbook chapters and review articles have been popular for use in teaching. He is valued at UW-Madison and nationally for his dedicated service and positive impact on committees and grant review panels. He is active in APS, International Society for Plant-Microbe Interactions, and American Society of Plant Biologists, where he continues to raise the profile of plant pathology within the broader plant biology community.

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